PDGFRA (Platelet Derived Growth Factor Receptor Alpha)

THAP9 lacks homologues in mice, highlighting potential human-specific mechanisms in oligodendrocyte development and emphasising the importance of studying species-specific factors in neurodevelopment. Our findings suggest that THAP9 is a novel human-specific regulator of oligodendrocyte maturation and opens new avenues for studying myelination disorders.

This improvement is likely due to the alleviation of synaptic structural and functional impairments in neurons. Our findings indicate that OPCs play a critical role in the pathogenesis of SAE, highlighting their potential as a novel therapeutic target for this condition.

In addition, virtual screening and drug sensitivity profiling identified several FDA-approved agents with potential relevance to CDH2-associated drug response. These findings indicate that CDH2 may serve as a candidate marker associated with cisplatin response in OC, and its association with immune cell infiltration provides further insight into mechanisms potentially underlying chemoresistance.

SAHA imposes a common anti-proliferative core but engages distinct lineage-conditioned risk modules in LUAD and LUSC-cell-cycle/migration-linked in LUAD and checkpoint/stress-linked in LUSC. These SAHA feature-sensing modules provide a mechanistic and clinically anchored framework for subtype-tailored HDAC-directed combinations and for future development of HDACi-aligned biomarkers in NSCLC.

The remaining patient had an unresectable tumor and received tyrosine kinase inhibitor therapy; however, sequential treatment with imatinib and sunitinib was clinically ineffective. However, their clinical behavior differs: D842Y-mutant GISTs consistently present as large, hypervascular tumors associated with acute complications. The therapeutic efficacy of tyrosine kinase inhibitors remains unclear, underscoring the need for further case accumulation to better define the clinical course and determine optimal treatment strategies for this rare subtype.

Approximately 9% of GBMs harbor targetable fusions, with five genes (FGFR3, MET, EGFR, NTRK2, PDGFRA) comprising 8%. These findings support multi-arm clinical trials to evaluate targeted therapies, potentially improving outcomes for molecularly defined GBM subgroups.

Molecular docking and 200 ns molecular dynamics simulations supported stable dual binding of 9d within the ATP-binding pocket of PDGFR and the catalytic cleft of CA IX. By simultaneously targeting oncogenic PDGFRA signaling and hypoxia-driven pH regulation (CA IX/XII), 9d represents a promising lead for preclinical development in PDGFR/CA IX/XII-driven leukemias.

P2, N=80, Recruiting, National Institute of Allergy and Infectious Diseases (NIAID) | N=60 --> 80

This study offers the first comprehensive overview of novel germline and somatic mutations in Tunisian HCC patients, representing a North African cohort, and highlights key molecular drivers of hepatocarcinogenesis. These findings support the integration of genetic profiling into clinical practice to enhance early diagnosis and guide personalized therapies.

Cross-organ single-cell integration prioritizes liver-selective stromal circuitry and nominates hepatocyte-FB axes (HGF-MET, AGT-AGTR1B) as plausible links between fibrogenic remodeling and a pro-tumorigenic niche, yielding testable hypotheses at the interface of regeneration, RAS biology, and tumor initiation.

While endoscopic resection is preferred for localized lesions, surgical intervention remains necessary in complex or obstructive cases. Understanding IFPs' molecular profile and cellular origin may refine future diagnostic and therapeutic approaches.

P=N/A, N=50, Active, not recruiting, National Health Research Institutes, Taiwan | Trial primary completion date: Dec 2025 --> Dec 2029